History and Physical Examination

History

Drug-induced lung diseases have no pathognomonic clinical, laboratory, physical, radiographic, or histologic findings. Thus, they are usually considered a diagnosis of exclusion (after eliminating infectious and other causes). Discontinuance of the offending agent is often followed by spontaneous improvement, whereas failure to appreciate the causal relationship between the drug and the pulmonary disease can lead to irreversible lung injury.

Unfortunately, certain aspects of drug-induced disease can hinder the recognition of this cause-and-effect relationship. Although many drugs can cause diffuse infiltrative lung disease, very few of the patients who receive such drugs experience this disease. In the case of cytotoxic drug-induced disease, respiratory symptoms may not appear until many weeks after the last exposure to the drug. Finally, the drugs that cause diffuse infiltrative lung disease are often prescribed for conditions that are themselves associated with an increased risk for the disease.

Thus, clinicians evaluating patients with possible drug-induced pulmonary symptoms must obtain a thorough drug exposure history, maintain a high index of suspicion, and use a systematic diagnostic approach to make the correct and firm diagnosis. Irey defined the following set of criteria for the diagnosis of drug reactions^[1]:

Correct identification of the drug, its dose, and its duration of administration
Exclusion of other primary or secondary lung diseases
Temporal eligibility: Appropriate latent period (exposure to toxicity)
Recurrence with rechallenge (not commonly performed)
Singularity of drug (ie, other drugs the patient is taking)
Remission of symptoms with removal of the drug
Characteristic pattern of reaction to a specific drug (perhaps previously documented)
Quantification of drug levels that confirm abnormal levels (especially for overdoses)
Degree of certainty of drug reaction (ie, causative, probable, or possible)

Physical examination

The physical examination findings of drug-induced lung disease are nonspecific. The patient may have crackles in the case of noncardiac pulmonary edema (NCPE), wheezes in the case of bronchospasm, and decreased breath sounds in pleural effusion. Furthermore, bibasilar “Velcro crackles” may be audible in cases of drug-mediated interstitial lung disease.

Differential Diagnoses

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Media Gallery

This image is a standard nonenhanced axial thoracic computed tomography scan. There is left lower lobe consolidation with some loss of volume and an air bronchogram. Transbronchial lung biopsy confirmed the diagnosis of cryptogenic organizing pneumonia (also known as bronchiolitis obliterans-organizing pneumonia [BOOP]).
Cryptogenic organizing pneumonia (also called bronchiolitis obliterans-organizing pneumonia [BOOP]) is often patchy and peribronchiolar. The proliferation of granulation tissue within small airways and alveolar ducts is excessive and is associated with chronic inflammation of the surrounding alveoli.
This image is a computed tomography scan of a patient with sarcoidosis. The pattern of multiple nodules seen here can manifest in patients taking medications that can cause granulomatous reactions.
This histology image from a lung biopsy specimen was obtained from the patient with sarcoidosis discussed in the previous image (see the computed tomography scan illustrating multiple nodules). Multiple areas of noncaseating granulomas are present. Drugs such as methotrexate, nitrofurantoin, procarbazine, and pentazocine can cause granulomatous lung disease.
This is a close-up histologic view of a noncaseating granuloma with a giant cell.
This histologic section of the lung shows diffuse alveolar damage in a patient with adult respiratory distress syndrome.
In usual interstitial pneumonitis or idiopathic pulmonary fibrosis, subpleural and paraseptal inflammation is present, with an appearance of temporal heterogeneity on histologic examination. Patchy scarring of the lung parenchyma and normal, or nearly normal, alveoli interspersed between fibrotic areas are the hallmarks of this disease. In addition, the lung architecture is completely destroyed.

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Author

Klaus-Dieter Lessnau, MD, FCCP Former Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory, Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Kevin Gerard G Lazo, DO Pulmonologist, Englewood Health Physician Network

Kevin Gerard G Lazo, DO is a member of the following medical societies: American College of Chest Physicians

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Thomas M Roy, MD Chief, Division of Pulmonary Disease and Critical Care Medicine, Quillen Mountain Home Veterans Affairs Medical Center; Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, Fellowship Program Director, James H Quillen College of Medicine, East Tennessee State University

Thomas M Roy, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Southern Medical Association, Wilderness Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Arshad Ali, MD Attending Physician, Department of Pulmonary and Critical Care Medicine, Mercy General Hospital of Sacramento

Arshad Ali, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose. M Frances J Schmidt, MD Chief of Pulmonary Medicine, Pulmonary Fellowship Program, Teaching Attending Physician, Department of Medicine, Interfaith Medical Center

M Frances J Schmidt, MD is a member of the following medical societies: American College of Chest Physicians and American College of Physicians

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment